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Cancer care (Y4) > 9- Haematological malignancy (Leukaemia) > Flashcards

9- Haematological malignancy (Leukaemia) Flashcards

1
Q

types of haematological malignancy

A
  • Leukaemia
  • Lymphoma
  • Myeloma
  • Myelodysplastic syndromes
  • Myeloproliferative neoplasms
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2
Q

haematopoietic lineage

A

common myleoid
common lymphoid

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3
Q

Haemopoietic stem cells

A

a cell isolated from the blood or bone marrow which can renew itself and differentiate into a variety of specialised cells

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4
Q

normal bone marrow aspirate and blood film

A
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5
Q

Pathophysiology of haematological malignancy

A

Loss of normal control on haemopoiesis
- Too many cells proliferating
- Cells don’t apoptosis when they should
- Cells don’t differentiate when they should
- The earlier in the haemopoiesis pathway that the mutation occurs the larger the variety of cells from that lineage. If mutation occurs at end of lineage- only one type of cell will proliferate

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6
Q

types of myeloid cancer

A

acute myeloid leukaemia
chronic myeloproliferative neoplasms

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7
Q

types of lymphoid cancer

A

Acute lymphoblastic leukaemia
Chronic lymphocytic leukaemia
Lymphoma

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8
Q

Leukaemia vs lymphoma

A

Leukaemia vs lymphoma
- Lots of cross over
- Leukaemia= cancers which affect mainly the bone marrow with or without release of circulating neoplastic cells into the blood
- Lymphoma = predominantly nodal or organ-based

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9
Q

haematological cancer presentation summary

A
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10
Q

constitutional symptoms

A

(any haem malignancy)
- Unintentional weight loss (>10%)
- Drenching night sweats
- Fever
- Pruritis

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11
Q

Symptoms of bone marrow failure

A

(any haem malignancy)
- Anaemia
- Thrombocytopenia
- Neutropenia

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12
Q

Symptoms of disease involvement

A

(any haem malignancy)
- Lumps
- Organomegaly
- Any site

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13
Q

Symptoms of hypercalcaemia (mostly myeloma, some lymphoma)

A
  • Fatigue
  • Abdo pain
  • N+V
  • Constipation
  • Headaches
  • Polydipsia/urea
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14
Q

Symptoms of hypervisosity

A

(uncommon, possible in Myeloma)
- - Headache
- Somnolence
- Visual disturbances

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15
Q

investigations for haemaotlogical malignancy

A

Bloods

  • FBC, U&Es, LFTs, CRP
  • Haematinics
  • Bone profile
  • Blood film
  • Virolgy (EBC, CMV, HIV)

Special bloods

  • LDH, urate B2M, PV
  • Ig +/- Serum Free Light Chain
  • PB immunophenotyping (flow cytometry)

Imaging

  • CT scan
  • PET scan (lymphoma /myeloma)
  • MRI spine/ pelvis (myeloma)

Invasive

  • Lymph node biopsy
    –> excisional biopsy the best
    –> if not do core biopsy (do not do FNAC)
  • Bone marrow aspirate and trephine (bone)
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16
Q

Diagnosis of haematological malignancy

A

Integrated approach
- Morphology
- Flow cytometry
- Immunohistochemistry
- Cytogenetics
- Mutational

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17
Q

management of haematological malignancy

A

MDT approach which depends on diagnosis and prognosis
- Chemotherapy
- New targeted therapies
- Precision medicine

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18
Q

leukaemia background

A
  • Malignancy of the stem cells in the bone marrow which causes an increase in number of white blood cells
  • Causes unregulated production of certain types of cells
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19
Q

Types of leukaemia can be classified depending on how rapidly they progress and the cell line affected

A

Speed
- Chronic
- Acute
Cell line
- Myeloid
- Lymphoid

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20
Q

peak age of ALL vs AML

A

ALL - 2-3yo
AML- <75yo

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21
Q

Pathophysiology of leukaemia

A
  • Genetic mutation in one of the precursor cell in the bone marrow leads to excessive production of a single type of abnormal white blood cell
  • Excessive production of one type of cell can lead to suppression of the other cell lines -> underproduction of all other types of cells -> pancytopenia
  • Pancytopenia is low:
    o RBC (anaemia)
    o WBC (leukopenia)
    o Platelets (thrombocytopenia)
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22
Q

risk factors for leukaemia

A

Radiation exposure, for example with an abdominal xray during pregnancy, is the main environmental risk factor for leukaemia.
There are several conditions that predispose to a higher risk of developing leukaemia:
- Down’s syndrome
- Kleinfelter syndrome
- Noonan syndrome
- Fanconi’s anaemia

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23
Q

Most common leukaemia’s

A

The types of leukaemia that affect children from most to least common are:

  • Acute lymphoblastic leukaemia (ALL) is the most common in children
  • Acute myeloid leukaemia (AML) is the next most common
  • Chronic myeloid leukaemia (CML) is rare
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24
Q

Acute Lymphoblastic Leukaemia: peak age of onset

A

Under 5s and over 45s

  • associated with DS
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25
Q

Chronic Lymphocytic Leukaemia: peak age of onset

A
  • Over 55ss
  • Most common leukaemia in adults
  • Associated with warm haemolytic anaemia, Richters transformation into lymphoma and smudge/smear cells
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26
Q

Acute Myeloid Leukaemia: peak age of onset

A
  • Over 75s
  • Most common acute adult leukaemia
  • Result of transformation from a myeloproliferative disorder
  • Associated with Auer rods
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27
Q

Chronic Myeloid Leukaemia: peak age of onset

A

over 65s
o 3 phases including a 5 year asymptomatic chronic phase
o Associated with philadelphia chromosome

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28
Q

mneumonic for learning peak ages for leukaemia

A

You can use the mnemonic “ALL CeLLmates have CoMmon AMbitions” to remember the progressive ages of the different leukaemia from 45-75 in steps of 10 years. Remember that ALL (the first in the mnemonic) most commonly affects children under 5 years.

Under 5 and over 45 – acute lymphoblastic leukaemia (ALL)
Over 55 – chronic lymphocytic leukaemia (CeLLmates)
Over 65 – chronic myeloid leukaemia (CoMmon)
Over 75 – acute myeloid leukaemia (AMbitions)

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29
Q

Acute and chronic leukaemia

A

Leukaemia is acute or chronic depending on how quickly it progresses.

Acute leukaemias
- tend to develop quickly and get rapidly worse if they are not treated.
- There are 2 main types of acute leukaemia:
o acute myeloid leukaemia (AML)
o acute lymphoblastic leukaemia (ALL)

Chronic leukaemias
- Develop slowly and tend to get worse slowly, over a long time.
- In chronic leukaemia the white blood cells are almost fully developed, but are not completely normal. They still work, but not as well as they should do at fighting infection. Your body makes too many of these abnormal white blood cells.
- There are 3 main types of chronic leukaemia:
o chronic lymphocytic leukaemia (CLL)
o chronic myeloid leukaemia (CML)
o hairy cell leukaemia

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30
Q

general presentation of leukaemia

A

The presentation of leukaemia is typically non-specific. Symptoms can include:

  • Persistent fatigue
  • Unexplained fever
  • Failure to thrive
  • Weight loss
  • Night sweats
  • Pallor (anaemia)
  • Petechiae and abnormal bruising (thrombocytopenia)
  • Unexplained bleeding (thrombocytopenia)
  • Abdominal pain
  • Generalised lymphadenopathy (>1cm)
  • Unexplained or persistent bone or joint pain
  • Hepatosplenomegaly
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31
Q

refferal for leukaemia

A

Any child with unexplained petechiae or hepatomegaly should be sent for specialist assessment. If leukopenia is suspected – urgent blood count within 48 hours.

32
Q

investigations for leukaemia

A

Any child with unexplained petechiae or hepatomegaly should be sent for specialist assessment. If leukopenia is suspected – urgent blood count within 48 hours.

Investigations to establish the diagnosis:

  • Full blood count, which can show anaemia, leukopenia, thrombocytopenia and high numbers of the abnormal WBCs
  • Blood film, which can show blast cells
  • Bone marrow biopsy
  • Lymph node biopsy
    Further tests may be required for staging:
  • Chest xray
  • CT scan
  • Lumbar puncture
  • Genetic analysis and immunophenotyping of the abnormal cells
33
Q

general management of leukaemia

A
  • Primary therapy: Chemotherapy
  • Other therapies
    o Radiotherapy
    o Bone marrow transplant
    o Surgery
34
Q

Complications of leukaemia

A
  • Failure to treat the leukaemia
  • Stunted growth and development
  • Immunodeficiency and infections
  • Neurotoxicity
  • Infertility
  • Secondary malignancy
  • Cardiotoxicity
35
Q

prognosis of leukaemia

A

Prognosis
The overall cure rate for ALL is around 80%, but prognosis depends on individual factors. The outcomes are less positive for AML.

36
Q

Acute lymphoblastic leukaemia background

A
  • Proliferation of lymphoid blasts- early cells (B or T cells)
  • Most common type of leukaemia to affect children
  • If not treated would cause death within a few weeks or months
37
Q

types of ALL

A
  • B-lymphoblastic leukemia (most common)
  • T-lymphoblastic leukemia
  • Philadelphia positive ALL (BCR-ABL1 mutation)
38
Q

Risk factors for ALL

A
  • More commonly diagnosed in children 0-4
  • But can be diagnosed in adults
  • M>F
39
Q

metastasis of ALL

A
  • Lymph nodes
  • Liver
  • Spleen
  • CNS
  • testicles
40
Q

Pathophysiology of ALL

A
  • Proliferation of lymphocytes occurs acutely- develops rapidly- in the bone marrow
  • These lymphocytes are not fully developed (blasts) and do not work properly
  • Abnormal cells build up in bone marrow and spill out into the blood and into other body parts
41
Q

Presentation of ALL

A
  • Pancytopenia since excess B cell proliferation causes them to replace other cell types being created in the bone
  • Fatigue
  • Fever
  • Infections
  • Weight loss
  • Breathlessness
  • Easy bruising
  • Swelling of lymph nodes
  • Bone pain
  • Lymphadenopathy
42
Q

blood film: ALL

A
  • When blast cells of lymphoid origin are ≥ 20% of marrow nucleated cells or ≥ 20% of non-erythroid cells when the erythroid component is > 50%.
  • Like hand held mirror
43
Q

investigations for ALL

A

Blood

  • FBC
  • U&Es
  • LFTs
    immunophenotyping

Invasive diagnostic

  • Bone marrow biopsy
  • Lumbar puncture e.g. To check if leukaemia cells have spread to CSF

Imaging

  • CXR
  • CT scan
  • MRI scan
  • US- lymph nodes, liver , spleen
  • PET-CT scan
44
Q

management of ALL

A

Management multi-drug

  • Multi-drug chemotherapy
    e.g. Vincristine, doxorubicin, cyclophosphamide, methotrexate
  • Steroids e.g. prednisolone or dexamethasone
  • Targeted cancer drugs
    e.g. Rituximab – monoclonal antibody
    e.g. imatinib- targets tyrosine kinase (for philadelphia positive patients)
  • Immunotherapy e.g. CAR T cell therapy
  • Radiotherapy
  • Stem cell or bone marrow transplants

Phases of treatment

  • Induction
  • Consolidation
  • Intensification
  • Maintenance
45
Q

Prognosis of ALL

A

For those younger than 15:
* almost 90 out of 100 (almost 90%) will survive their leukaemia for 5 years or more after diagnosis
For those aged between 15 and 39:
* almost 65 out of 100 (almost 65%) will survive their leukaemia for 5 years or more after diagnosis
For those who are 40 or older:
* around 20 out of 100 (around 20%) will survive their leukaemia for 5 years or more after diagnosis

46
Q

chronic lymphocytic leukaemia background

A
  • Proliferation of mature B lymphocytes- from lymphoid blood stem cells
  • Can have nodal and splenic disease
  • Immune dysregulation e.g. AIHA, ITP
    o Associated with autoimmune conditions
  • Develops slowly and gets worse over time
  • Relapsing and remitting disease
  • CLL can transform to high-grade lymphoma -> Richters transformation
47
Q

Richters transformation

A

This is when the CLL changes (transforms) into a rare type of non-Hodgkin lymphoma, usually diffuse large B cell lymphoma.

48
Q

RF for CLL

A

Risk factors
- Older
- M>F

49
Q

presentation of of CLL

A
  • Low immunoglobulins causing infection
  • Anaemia
  • Bleeding
  • Weight loss
  • Warm autoimmune haemolytic anaemia
  • Swollen lymph glands
  • Bleeding or bruising
  • Bone pain
  • Night sweats
50
Q

staging ofr CLL

A
  • Rai/Binet staging
51
Q

blood film: CLL

A
52
Q

investigations for CLL

A

Blood

  • FBC
  • U&Es
  • LFTs
  • immunophenotyping

Invasive

  • Bone marrow biopsy
  • Lumbar puncture
    (To check if leukaemia cells have spread to CSF)

Imaging

  • CXR
  • CT scan
  • US- lymph nodes, liver , spleen
  • Testing lymph nodes for CL
53
Q

Management of CLL

A

multi-drug
- Targeted drug therapy e.g Ibrutinib
- Chemotherapy

54
Q

prognosis of CLL

A

Prognosis
- 85% survival after 5 years

55
Q

ALL vs CLL

A

ALL is an aggressive, fast-moving leukemia which requires immediate, intensive (often inpatient) treatment, frequently followed by allogeneic stem cell transplantation.” On the other hand, “CLL is typically a slow-moving, chronic process that may not require treatment for years

56
Q

Acute myeloid leukaemia background

A

Most common acute adult leukaemia

  • Classification based mainly on cytogenic abnormalities and morphology
  • Can be the result of transformation from a myeloproliferative disorder such as polycythaemia rubra vera or myelofibrosis
  • Progresses rapidly without treatment
  • Needs immediate medical attention
57
Q

AML can be the result of

A

It can be the result of a transformation from a myeloproliferative disorder such as polycythaemia ruby vera or myelofibrosis.

58
Q

risk factors AML

A
  • No obvious risk factors
  • Men
  • Older age
  • Smoking
  • Radiation
  • Other blood cancers
59
Q

presentation of AML

A

Pancytopenia
- Anaemia – fatigue SoB
- Neutropenia – infection
- Thrombocytopenia - bruising

60
Q

blood film for AML

A

A blood film will show a high proportion of blast cells (LARGE CELL AND NUCLEUS TAKES UP MOST SPACE). These blast cells can have rods inside their cytoplasm that are named Auer rods.

61
Q

Auer rods

A
62
Q

investigations for AML

A

Blood tests: FBC (bone marrow function), UEs, LFTs, Haematinics (ferritin), LDH (cell turnover), bone profile, virology (CMB, EBV, HIV), immunoglobulins (IgM, IgG)
- Blood film

Invasive : bone marrow biopsy

Imaging
- CT- neck, chest, abdo pelvis
- MRI
- US
- PET (staging)

63
Q

management of AML

A

Chemotherapy
- remission inductio
- consolidation (post-remission therapy)
- maintenance

64
Q

Chronic myeloid leukaemia background

A
  • High WBC count and massive spleen
  • Caused by cytogenetic translocation (BCR- ABL1 Philadelphia)
  • Increase in all myeloid cells including basophils, neutrophils, eosinophils, monocytes)
  • Can progress to AML
  • Chronic phase -> accelerated -> blast crisis
    o Where there is a sudden increase in blast cells in bone marrow and blood
  • Takes longer to develop than AML- people can live for many years
  • Always think CML if you see BCR-ABL1
65
Q

RF for CML

A

Risk factors
- BCR-ABL1 mutation (Philadelphia chromosome)
- Exposure to radiation
- Increased age

66
Q

presentation of CML

A

Presentation
- High white cell count
- Splenomegaly
o Early satiety due to spleen compressing stomach
- Getting infections more than usually
- Related to deficiency in:
o RBC: Fatigue/ SoB
o Platelet: Abnormal bleeding
- Weight loss
- Night swats
- Bone pain

67
Q

blood film CML

A

will show a variety of myeloid cells including: basophils, monocytes, eosinophils, lymphocytes etc

68
Q

phases of CML

A

Chronic myeloid leukaemia has three typical phases: the chronic phase, the accelerated phase and the blast phase. The chronic phase can last around 5 years, is often asymptomatic and patients are diagnosed incidentally with a raised white cell count.

The accelerated phase occurs where the abnormal blast cells take up a high proportion of the cells in the bone marrow and blood (10-20%). In the accelerated phase patients become more symptomatic, develop anaemia and thrombocytopenia and become immunocompromised.

The blast phase follows the accelerated phase and involves an even high proportion of blast cells and blood (>30%). This phase has severe symptoms and pancytopenia. It is often fatal.

69
Q

investigations for CML

A

- Blood tests: FBC (bone marrow function), UEs, LFTs, haemitinics (ferritin), LDH (cell turnover), bone profile, virology (CMB, EBV, HIV), immunoglobulins (IgM, IgG)
- Blood film
- Bone marrow biopsy
- imaging: CT, MRI, PET

70
Q

Lactate dehydrogenase (LDH)

A

represents high tissue turnover e.g. released from cells breaking down
is a blood test that is often raised in leukaemia but is not specific to leukaemia. It can be raised in other cancers and many non-cancerous diseases.

71
Q

The cytogenetic change that is characteristic of CML is

A

the Philadelphia chromosome, which is a translocation of genes between chromosome 9 and 22: it is a t(9:22) translocation.

72
Q

management of CML

A

imatinib - tyrosine kinase inhibitor
- works on the BCR-ABL mutation
- least side effets and most effective

73
Q

how is CML disease monitored

A

Minimal Residual Disease - measure BCR-ABL transcripts in the blood

74
Q

if imatinib not working for CML

A

change to a different tyrosine kinase inhibitor

75
Q

in CML, white blood cells can be very high, what the potential complications

A

It can cause a stroke or breathing problems that could lead to death. Doctors treat this syndrome by adding fluid to the blood and using drugs to reduce the neutrophils in the blood

-> WCC paluqes can form in kidneys and eyes

Cancer care (Y4) (30 decks)

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